SETDB1 overexpression

In conclusion, subcellular localization of cytoplasmic SETDB1 may be a pivotal factor in breast cancer progression. The present study offers valuable insight into the novel functions and mechanisms of cytoplasmic SETDB1.

SETDB1 is highly expressed in colorectal cancer and plays an important role in the invasion and metastasis through the Wnt/β-catenin pathway. It does so by direct methylation of β-catenin. This novel SETDB1/Wnt/β-catenin pathway provides a new strategy for the treatment of colorectal cancer.

In conclusion, the findings of the present study indicated that SETDB1 promoted lenalidomide resistance in MM cells by promoting EMT and the PI3K/AKT signaling pathway. Thus, SETDB1 may be a potential therapeutic target for MM.

SETDB1 silencing upregulates SLC17A7 levels. SETDB1 has an oncogenic role in pHGG.

We have demonstrated that SETDB1 OE promotes gastric carcinogenesis through multiple signaling pathways including EMT and immune evasion. It could lead to new therapeutic strategies to clarify SETDB1’s roles in tumorigenesis or immune evasion.

Our findings revealed that Sp1 transcriptionally inhibited HPGD via SETDB1 in a β-catenin-dependent manner and promoted the proliferation and metastasis of GC cells.

C5aR1 promotes the development of CRC and accelerates the EMT process. Furthermore, C5aR1 may involve in the regulation of Wnt/β-catenin pathway in CRC.

This study suggests that the PELP1/SETDB1 axis play an important role in aberrant Akt activation and serves as a novel target for treating endocrine therapy resistance in breast cancer.

SETDB1 expression in myeloma cells was positively correlated with CD56dim natural killer cells but negatively correlated with infiltrating levels of type17 T helper cells, effector memory CD8 T cells, activated dendritic cells, and natural killer T cells from whole bone marrow (WBM) biopsies. Taken together, these results indicated that SETDB1 could be used as a novel biomarker for predicting the prognosis of MM patients.

Our findings indicated that SETDB1 might play a carcinogenic role by increasing the infiltration of immune cell and influencing immune checkpoint expression. This study suggested that miR-29a-3p can mediate the expression of SETDB1 with poor prognosis and tumor immune infiltration in BRCA.

Accordingly, we review several methods that have been used to target SETDB1, such as using Mithramycin A, Mithralog EC-8042, 3'-deazaneplanocin A (DZNep), and paclitaxel. Finally, we conclude by highlighting remaining gaps in knowledge and challenges surrounding SETDB1. Ultimately, our review captures the wide scope of findings on SETDB1's history, function, its implications in cancer, and provides suggestions for future research in the field.